ライフサイエンスコーパス: leading strand

1 cess is triggered, ejecting Pol delta on the leading strand.

2 epair to the continuously replicated nascent leading strand.

3 ccessible 3'-OH group in the template of the leading strand.

4 ' efficiency than 'those that anneal to' the leading strand.

5 t with more common template switching on the leading strand.

6 as for fusion of telomeres replicated by the leading strand.

7 ff at the Top1 cleavage complex sites on the leading strand.

8 ase checkpoint response to DNA damage on the leading strand.

9 nt lagging strand at the branch point but no leading strand.

10 lagging strand replication compared with the leading strand.

11 on forks where there is a gap in the nascent leading strand.

12 lizes fork structures with large gaps in the leading strand.

13 ts Pol epsilon against RFC inhibition on the leading strand.

14 ch higher rate when (TG)2 was on the nascent leading strand.

15 rand and CMG enforces quality control on the leading strand.

16 lta is slow and distributive with CMG on the leading strand.

17 us DNA synthesis of both the lagging and the leading strands.

18 immediate effect on the rate of extension of leading strands.

19 n of dGTP decreased the rate of extension of leading strands.

20 rmediates come from both the lagging and the leading strands.

21 3/iCy5) chromophore pairs in the lagging and leading strands.

22 d DNA structures, and translocates along the leading strand (3' to 5' direction).

23 repair events nick continuously synthesized leading strands after synthesis, producing the observed

24 RR pathway when the lesion is located on the leading strand and a role for the Rad52 pathway when the

25 gle ribonucleotide at the 5' end of both the leading strand and at least the first Okazaki fragment i

26 ands that are extended by Pol epsilon on the leading strand and by Pol delta on the lagging strand.

27 n resulting in continuous replication on the leading strand and discontinuous replication on the lagg

28 CMG (Cdc45-MCM-GINS) helicase surrounds the leading strand and is proposed to recruit Pol epsilon fo

29 DNA replication, initiating synthesis of the leading strand and of each Okazaki fragment on the laggi

30 eukaryotic cells, Pol epsilon being the main leading strand and Pol delta the lagging strand DNA poly

31 for specific targeting of Pol epsilon to the leading strand and provides clear mechanistic evidence f

32 tinuous polymerization of nucleotides on the leading strand and the discontinuous synthesis of DNA on

33 r substrates that contain no gap between the leading strand and the duplex portion of the fork, as de

34 he difference between the replication of the leading strand and the lagging strand--to establish an a

35 Their increased abundance on leading strands and decreased abundance on lagging stran

36 case binds Pol epsilon and tethers it to the leading strand, and PCNA (proliferating cell nuclear ant

37 jority of bacterial genes are located on the leading strand, and the percentage of such genes has a l

38 ination, translesion replication (TR) on the leading strand, and TR on the lagging strand.

39 r replication forks collide with an ICL, the leading strand approaches to within one nucleotide of th

40 a model fork, than to the 3' single-stranded leading strand arm.

41 lex lagging-strand arm and a single-stranded leading-strand arm.

42 nd CMG helps to stabilize Pol epsilon on the leading strand as part of a 15-subunit leading-strand ho

43 NA polymerase epsilon, which synthesises the leading strand at DNA replication forks.

44 NA polymerase epsilon, which synthesizes the leading strand at replication forks and is an important

45 tes with the DNA polymerase that acts on the leading strand at replication forks, suggesting a potent

46 pair is to unhook the damage by incising the leading strand at the 3' side of an ICL lesion.

47 inding with primer synthesis to initiate the leading strand at the viral origin and each Okazaki frag

48 er-strand positive effect on the rate of the leading strand based in its interaction with the replica

49 coli postulates continuous synthesis of the leading strand, based on in vitro experiments with purif

50 is important for fitness are selected to the leading strand because this reduces the duration of thes

51 The leading strand bias was lost in the absence of exonuclea

52 central hole of the hexagonal helicase, the leading strand binds to the "outside" surfaces of subuni

53 Hence, Pol epsilon is active with CMG on the leading strand, but it is unable to function on the lagg

54 no-acid-changing mutations tend to be on the leading strand, co-oriented with replication.

55 mma S, supports the formation of an isolable leading strand complex that loads and replicates the lag

56 more mismatches during replication than its leading-strand counterpart, polymerase epsilon; that mos

57 some is able to directly replicate through a leading-strand cyclobutane pyrimidine dimer (CPD) lesion

58 that the creation of a flap at the site of a leading strand discontinuity could, in principle, allow

59 ons without dissociating by synthesizing the leading strand discontinuously.

60 lling-circle mechanism that exclusively uses leading strand displacement synthesis.

61 ody of evidence specifies Pol epsilon as the leading strand DNA polymerase and Pol delta as the laggi

62 Unexpectedly, the leading strand DNA polymerase epsilon (Polepsilon) arriv

63 activation and support a model in which the leading strand DNA polymerase is recruited prior to orig

64 role after initiation, because it links the leading strand DNA polymerase to the Cdc45-MCM-GINS heli

65 llowing completion of DNA replication by the leading strand DNA polymerase, and associated histone mo

66 Finally, recruitment of lagging but not leading strand DNA polymerases depends on Mcm10 and DNA

67 RNA-DNA fragments for priming of lagging and leading strand DNA replication in eukaryotes.

68 cient proofreading or mismatch repair during leading strand DNA replication.

69 DNA polymerase (Pol) epsilon mediates leading strand DNA replication.

70 agility and the first known role for FEN1 in leading strand DNA replication.

71 psilon (Pol epsilon) carries out the bulk of leading strand DNA synthesis at an undisturbed replicati

72 extends into the adjacent Delta2 site, where leading strand DNA synthesis begins.

73 Leading strand DNA synthesis requires functional couplin

74 2 protein is required for helicase-dependent leading strand DNA synthesis when the helicase is loaded

75 ying a major role in fork progression during leading strand DNA synthesis, we propose that TWINKLE is

76 tic increase in the rate and processivity of leading strand DNA synthesis.

77 ng to the recombination-primed initiation of leading strand DNA synthesis.

78 omes showed loss of telomeres synthesized by leading strand DNA synthesis.

79 unwinding of the duplex prior to subsequent leading strand DNA synthesis.

80 cation proceeds with continuous synthesis of leading-strand DNA and discontinuous synthesis of laggin

81 At the site of a leading-strand DNA lesion, forks may stall and leave the

82 referential for repair of mismatches made by leading-strand DNA polymerase epsilon as compared to lag

83 hesis and to a surprising obstruction of the leading-strand DNA polymerase in vitro, pointing to role

84 , the replicative DNA helicase, MCM, and the leading-strand DNA polymerase, Pol epsilon, move beyond

85 nit of DNA polymerase epsilon, essential for leading-strand DNA replication and for the checkpoint.

86 n addition to proofreading and MMR influence leading-strand DNA replication fidelity.

87 us (AAV) replicates its DNA exclusively by a leading-strand DNA replication mechanism and requires co

88 that DNA polymerase epsilon participates in leading-strand DNA replication.

89 lagging-strand holoenzyme can occur without leading-strand DNA replication.

90 ese three altered helicases support rates of leading-strand DNA synthesis comparable to that observed

91 gene 5 DNA polymerase (gp5) are crucial for leading-strand DNA synthesis mediated by the replisome o

92 DNA faster, which allows it to keep up with leading-strand DNA synthesis overall.

93 t the interactions essential to initiate the leading-strand DNA synthesis remain unidentified.

94 -type fusions involving telomeres created by leading-strand DNA synthesis, reflective of a failure to

95 ease to process telomere ends synthesized by leading-strand DNA synthesis, thereby creating a termina

96 nthesis mediated by T7 DNA polymerase during leading-strand DNA synthesis.

97 specifically at those telomeres generated by leading-strand DNA synthesis.

98 G(2), specifically at telomeres generated by leading-strand DNA synthesis.

99 eration of a 3' overhang after completion of leading-strand DNA synthesis.

100 izes, and nicks the Ori sequence to initiate leading-strand DNA synthesis.

101 lomeres, namely, those that were produced by leading-strand DNA synthesis.

102 primary function is to synthesize DNA at the leading strand during replication.

103 oposed to induce resection that protects the leading-strand ends from NHEJ when TRF2 is absent.

104 s active despite its connection to a stalled leading strand enzyme.

105 ypothesis that DNA polymerase epsilon is the leading-strand enzyme, we observed no idling by this enz

106 establishment of repressive chromatin on the leading strand following DNA synthesis may depend upon t

107 The rate of the leading strand fork movement was at an average of approx

108 to guard against occasional slippage of the leading strand from the core channel.

109 To differentiate leading strands from lagging strands, the circular parts

110 mPol), plays a crucial role in the bypass of leading strand G4 structures.

111 Conversely, ODNs that anneal to the leading strand generate fewer editing events although th

112 ments in the lagging strand or breaks in the leading strand generated by the mismatch-activated endon

113 efficient strand and (iv) the percentage of leading-strand genes in an bacterium can be accurately e

114 and proliferating cell nuclear antigen, long leading strands (>10 kb) are produced.

115 rimosome composed of gp41, gp61, and gp59; a leading strand holoenzyme composed of gp43, gp44/62, and

116 orescence microscopy, that the inhibition of leading-strand holoenzyme progression by gp59 is the res

117 n the leading strand as part of a 15-subunit leading-strand holoenzyme we refer to as CMGE.

118 ibosome have higher preferences to be on the leading strands; (ii) genes of some functional categorie

119 e mutations faster than those encoded on the leading strand in Bacillus subtilis.

120 ly proposed discontinuous replication of the leading strand in E. coli.

121 erases in replication of the lagging and the leading strands in human cells, respectively.

122 from the initial fork was elongated as a new leading-strand in the retrograde direction without laggi

123 We show that leading-strand initiation preferentially occurs within a

124 Due to the anti-parallel nature of DNA, the leading strand is copied continuously, while the lagging

125 m the unhooked lesion ("insertion"), and the leading strand is extended beyond the lesion ("extension

126 polarity of duplex DNA necessitates that the leading strand is replicated continuously whereas the la

127 Although the leading strand is synthesized continuously, the lagging

128 bstacles in its path and may explain why the leading strand is synthesized discontinuously in vivo.

129 gression, even when the 3'-OH of the nascent leading strand is unavailable.

130 ting the lagging strand and G templating the leading strand; (iv) there is a strong bias for transiti

131 tion forks that collapse upon encountering a leading strand lesion are reactivated by a recombinative

132 ed for the DNA repair pathways described for leading strand lesion bypass and synthesis-dependent str

133 erase IV came at the expense of the inherent leading strand lesion skipping activity of the replisome

134 gment is synthesized beyond the point of the leading strand lesion.

135 structure of a replication fork stalled at a leading strand lesion.

136 the known structures of a fork stalled at a leading-strand lesion, we show here that RecA protein of

137 daughter-strand gaps are generated opposite leading-strand lesions during the replication of ultravi

138 9 cluster is required to facilitate telomere leading strand maturation and prevention of genomic inst

139 by producing 3 mature microRNAs: 1 from the leading strand (miR-146a), and 2 from the passenger stra

140 n fork structures, the presence of a nascent leading strand, modelling the effects of replication arr

141 Incisions are triggered when the nascent leading strand of a replication fork strikes the ICL Her

142 uplex during unwinding, corresponding to the leading strand of a replication fork.

143 is skewed so that it is predominantly on the leading strand of chromosomal replication.

144 a strong bias for genes to be encoded on the leading strand of DNA, resulting in coorientation of rep

145 marily incorporated on the newly synthesized leading strand of nuclear DNA and were present upstream

146 In addition, genes on the leading strand of replication were on average more G+T-r

147 In bacteria, most genes are on the leading strand of replication, a phenomenon attributed t

148 Most genes in bacteria are encoded on the leading strand of replication.

149 is defective, ribonucleotides in the nascent leading strand of the yeast genome are associated with r

150 e nascent single-stranded DNA (ssDNA) of the leading strand on active forks than on stalled forks.

151 uct was placed on the template either to the leading strand or to the lagging strand of nascent DNA w

152 s from a central origin produces unpaired 3'-leading-strand overhangs at the telomeres of replication

153 en suggested that the daughter strand of the leading strand partially dissociates from the parent str

154 tably as forks approach each other, and that leading strands pass each other unhindered before underg

155 der at the fork prevents the coupling of the leading strand polymerase and the helicase, unless the p

156 The leading strand polymerase and the primosome also associa

157 rk is probably important for stabilizing the leading strand polymerase interactions with authentic re

158 e helicase and both DNA polymerases when the leading strand polymerase is blocked.

159 e polarity of DNA duplex, replication by the leading strand polymerase is continuous whereas that by

160 Upon ATP gamma S-induced dissociation, the leading strand polymerase is refractory to disassembly a

161 Furthermore, the blocked leading strand polymerase remains stably bound to the re

162 ein-DNA complexes contain ssDNA ahead of the leading strand polymerase.

163 tly assigned polymerase (Pol) epsilon as the leading strand polymerase.

164 result of a complex formed between gp59 and leading-strand polymerase (gp43) on DNA that is instrume

165 d polymerase does not compromise helicase or leading-strand polymerase activity.

166 The leading-strand polymerase advances in a continuous fashi

167 The helicase binds the leading-strand polymerase directly, but is connected to

168 nthesis, involves physical separation of the leading-strand polymerase from the replisome.

169 Instead, the leading-strand polymerase remains limited by the speed o

170 ication likely results from a failure of the leading-strand polymerase still associated with the DNA

171 ntiparallel nature of duplex DNA permits the leading-strand polymerase to advance in a continuous fas

172 s, the Cdc45-MCM-GINS (CMG) helicase and the leading-strand polymerase, Pol epsilon, form a stable as

173 he replisome because of its contact with the leading-strand polymerase.

174 ase so that it advances in parallel with the leading-strand polymerase.

175 ase so that it advances in parallel with the leading-strand polymerase.

176 ent from S-phase replication, involving only leading-strand polymerization.

177 120- or 240-nt DNA substrates annealed to a leading-strand primer.

178 l elongation of the RNA, which serves as the leading-strand primer.

179 2 to 0.6 kb) were significantly shorter than leading strand products ( approximately 2 to 10 kb), and

180 plate, we obtained robust DNA synthesis with leading strand products of >20,000 nucleotides and laggi

181 itiated downstream of an unrepaired block to leading-strand progression, even when the 3'-OH of the n

182 dditional forks collide and displace nascent leading strands, providing yet more potential targets fo

183 tinue DNA synthesis without impediment, with leading strand re-priming by DnaG.

184 he conclusion that Polepsilon is the primary leading strand replicase and that Poldelta is restricted

185 ibutes to genomic stability via its roles in leading strand replication and the repair of damaged DNA

186 on protein, is required for normal, complete leading strand replication at telomeres.

187 he apparent lack of Poldelta contribution to leading strand replication is due to differential mismat

188 op, previously characterized in vitro at the leading strand replication origin (OH), is isolated as a

189 A polymerase epsilon, which is implicated in leading strand replication, incorporates one rNMP for ev

190 h recent evidence implicating Pol epsilon in leading strand replication, these data support a model o

191 lagging-strand synthesis leads to pausing of leading-strand replication and the introduction of the i

192 ent formation of the imprint occur after the leading-strand replication complex has passed the site o

193 he identity of the major polymerase used for leading-strand replication is uncertain.

194 's mutational footprint suggests: (i) during leading-strand replication pol I is gradually replaced b

195 is enriched at lagging strands compared with leading-strand replication.

196 The minimal reconstituted leading-strand replisome requires 24 proteins, forming t

197 rc1-Tof1-Csm3 (MTC) enhances the rate of the leading-strand replisome threefold.

198 d characterize their interaction with active leading-strand replisomes.

199 es further along the lagging strand than the leading strand, resulting in the exposure of long stretc

200 aucity of pol3-L612M-generated errors on the leading strand results from their more proficient remova

201 plication fork structures with and without a leading strand single-stranded DNA gap.

202 This is the first direct proof of leading strand-specific replication by human POLE, which

203 ata reveal the first molecular mechanism for leading strand-specific telomere fragility and the first

204 These data suggest that FEN1 limits leading strand-specific telomere fragility by processing

205 y, but not DNA repair activities, results in leading strand-specific telomere fragility.

206 The leading strand subsequently resumes synthesis, stalls ag

207 highly transcribed genes, are encoded on the leading strand such that transcription and replication a

208 obust on fork structures with no gaps in the leading strand, such as is found at the junction of a D

209 g strand synthesis decreases the rate of the leading strand, suggesting that lagging strand operation

210 the side channel, but in the open state, the leading strand surprisingly interacts with Cdc45.

211 -catalyzed DNA unwinding stimulate decoupled leading strand synthesis but not coordinated leading and

212 Leading strand synthesis by wild type T4 polymerase is s

213 e results support the model of discontinuous leading strand synthesis in E. coli.

214 he protein-protein interface stabilizing the leading strand synthesis involves two distinct interacti

215 synthesis produce equal amounts of DNA, (ii) leading strand synthesis proceeds faster under condition

216 Leading strand synthesis requires PolC plus ten proteins

217 urrent but unsubstantiated model posits only leading strand synthesis starting at a nick near one cov

218 However, 32 protein is not required for leading strand synthesis when helicase is loaded, less e

219 g strand synthesis proceeds much faster than leading strand synthesis, explaining why gaps between Ok

220 the lagging strand polymerase is faster than leading strand synthesis, indicating that replisome rate

221 he telomere, which copy the G-rich strand by leading strand synthesis, moved slower through the telom

222 tion of these replication complexes supports leading strand synthesis.

223 d, abortive DNA products are observed during leading strand synthesis.

224 ty of the polymerase-helicase complex during leading strand synthesis.

225 fusions involve only telomeres generated by leading strand synthesis.

226 ormed during copying of the G-rich strand by leading strand synthesis.

227 apping functions of BLM and WRN helicase for leading strand synthesis.

228 r genomic replication and is responsible for leading strand synthesis.

229 s the RNA transcript as a primer to continue leading-strand synthesis after the collision with RNA po

230 lacked dCMP; thus, no dCTP was required for leading-strand synthesis and no dGTP for lagging-strand

231 enase) can replace the T4 DNA polymerase for leading-strand synthesis but not for well coordinated la

232 Specifically targeting leading-strand synthesis by decreasing the concentration

233 assay to provide real-time visualization of leading-strand synthesis by the S. cerevisiae replisome

234 , controlled by a molecular brake that halts leading-strand synthesis during primer synthesis.

235 and lagging-strand DNA synthesis by blocking leading-strand synthesis during the primosome assembly.

236 servation suggests a mechanism that prevents leading-strand synthesis from outpacing lagging-strand s

237 devoid of unwinding activity alone, supports leading-strand synthesis in the presence of T7 DNA polym

238 Leading-strand synthesis is then reinitiated downstream

239 e show that replication can be restarted and leading-strand synthesis re-initiated downstream of an u

240 As expected, leading-strand synthesis stalls prematurely in the absen

241 occur when DNA polymerase epsilon catalyzes leading-strand synthesis together with its processivity

242 en these DNA polymerases also contributes to leading-strand synthesis under conditions of replicative

243 rprisingly also plays a role in establishing leading-strand synthesis, before DNA polymerase epsilon

244 DNA polymerase delta can support leading-strand synthesis, but at slower rates.

245 d and is proposed to recruit Pol epsilon for leading-strand synthesis, but to date a direct interacti

246 thesis proceeds downstream in the absence of leading-strand synthesis, involves physical separation o

247 ision at ribonucleotides incorporated during leading-strand synthesis.

248 ng coordination with the continuous and fast leading-strand synthesis.

249 hangs generated at the telomeres produced by leading-strand synthesis.

250 e transient pausing of the highly processive leading-strand synthesis.

251 enerated by lagging-strand synthesis than by leading-strand synthesis.

252 y monitoring the kinetics of loop growth and leading-strand synthesis.

253 y' during ongoing DNA synthesis and that the leading-strand T7 replisome does not pause during primer

254 Leading-strand telomere ends were not prone to fuse in t

255 MRE11 can also protect newly replicated leading strand telomeres from NHEJ by promoting 5' stran

256 Moreover, analysis of leading strand telomeres revealed that a significant fra

257 ingle-stranded overhangs at newly replicated leading-strand telomeres to protect them from engaging t

258 its nuclease activity is required to protect leading-strand telomeres.

259 NM1B complex formation and the protection of leading-strand telomeres.

260 TRF1 binds BLM to facilitate lagging but not leading strand telomeric DNA synthesis.

261 d5 pathway when the lesion is located on the leading strand template and for the Rad52 pathway when t

262 A DPC on the leading strand template arrests the replisome by stallin

263 DNA endonuclease(s) unhooks an ICL from the leading strand template at a stalled replication fork si

264 ith the Escherichia coli replisome to bypass leading strand template damage, despite the fact that bo

265 ding of RecA on ssDNA regions exposed on the leading strand template of damaged forks, and do so by u

266 e effect of a noncoding DNA lesion in either leading strand template or lagging strand template on th

267 ssDNA must be exposed on the leading strand template to elicit this cooperativity, in

268 d when cloned in orientation II (CAGG on the leading strand template) rather than I and when cloned p

269 s observed where orientation II (CAGG on the leading strand template) was more prone to recombine.

270 of the G4 is dependent on it residing on the leading strand template, but is independent of its in vi

271 ical in targeting accessory helicases to the leading strand template, indicating an important role fo

272 eplisome encounters a blocking lesion in the leading strand template, the replication fork only trave

273 trand template much more readily than on the leading strand template.

274 s no evidence for a new priming event on the leading strand template.

275 e lagging-strand template (LGST) than in the leading-strand template (LDST).

276 e the replisome is stalled by collision with leading-strand template damage.

277 e the replisome is stalled by collision with leading-strand template damage.

278 in extensive degradation of the nascent and leading-strand template DNA and a loss of replication fo

279 se association with the helicase to copy the leading-strand template in a continuous manner while the

280 site-specific, cyclobutane pyrimidine dimer leading-strand template lesion provides only a transient

281 e of a collision between the replisome and a leading-strand template lesion remains poorly understood

282 erichia coli replisome transiently stalls at leading-strand template lesions and can either reinitiat

283 tions reveal that the replisome can tolerate leading-strand template lesions without dissociating by

284 ansiently when it encounters a lesion in the leading-strand template, skipping over the damage by rei

285 ing-strand template and at least once on the leading-strand template.

286 xposure of long stretches of single-stranded leading-strand template.

287 aB and Rep translocate along the lagging and leading strand templates, respectively, interact physica

288 ons, should be more strongly selected to the leading strand than singleton transcripts.

289 eplicative helicase enables synthesis of the leading strand to continue.

290 icase activation, the h2i clamps down on the leading strand to facilitate strand retention and regula

291 some prior to replication fork runoff on the leading strand to generate DSBs.

292 lesion bypass involves advance of a nascent leading strand to within one nucleotide of the ICL, foll

293 Eviction of the stalled helicase allows leading strands to be extended toward the ICL, followed

294 tial genes, which are strongly biased to the leading strand, to occur in operons.

295 ns-anti-benzo[a]pyrene-N(2)-dG lesion on the leading strand was efficiently and quickly recovered via

296 ting the lagging strand and T templating the leading strand, whereas G:C > A:T transitions preferenti

297 ier that Pol delta-PCNA is suppressed on the leading strand with CMG.

298 he lagging strand compared with those on the leading strand, with this difference being primarily in

299 tion or the rate of the fork movement on the leading strand within the first 30 s of the reaction.

300 his action results in a discontinuity in the leading strand, yet the replisome remains intact and bou